巻号一覧
3 巻 (1980)
- 6 号 p. 343-
- 5 号 p. 231-
- 4 号 p. 173-
- 3 号 p. 113-
- 2 号 p. 57-
- 1 号 p. 1-
3 巻, 4 号
選択された号の論文の7件中1～7を表示しています
- |<
- <
- 1
- >
- >|
-
畔柳 武雄1980 年 3 巻 4 号 p. 173-180
発行日: 1980/09/30
公開日: 2009/01/22
ジャーナル フリーPDF形式でダウンロード (548K) -
小出 幸夫, 淡嶋 史佳, 赤座 達也, 吉田 孝人1980 年 3 巻 4 号 p. 181-185
発行日: 1980/09/30
公開日: 2009/01/22
ジャーナル フリーヒト抗原呈示細胞はPPDパルスされることにより自己の感作T細胞および一部のアロのT細胞を活性化することが認められた. PPDパルス抗原呈示細胞上のHLA-A, -Bそして-DR抗原を抗血清で選択的に被う実験で, HLA-DR抗原に対する抗血清のみが抗原呈示能を阻止することから,感作T細胞は抗原呈示細胞上のPPDとDR抗原を同時に認識することが判明した.このことはアロのT細胞の活性化にはHLA-DR抗原の少なくとも1つを抗原呈示細胞と共有していることが必要であることを示している.抄録全体を表示PDF形式でダウンロード (243K) -
畔柳 武雄, 蔵 和夫, 荒尾 俊夫, 藤谷 貴文, 荘 茂, 田中 和也1980 年 3 巻 4 号 p. 186-195
発行日: 1980/09/30
公開日: 2009/01/22
ジャーナル フリーA marked decrease of T lymphocytes and Tγ was demonstrated in 8 patients with IBL. Null lymphocytes increased makedly in IBL. Null lymphocytes were present in the Fr I fractionated by gumi accaci density gradient centrifugation of blood lymphocytes. The PHA blastoid transformation of IBL blood lymphocytes slightly decreased. A marked decrease of Ts was demonstrated in blood and lymphnode lymphocytes in IBL. The development of cIg+ cells by PWM stimulation from IBL lymphnode B lymphocytes was demonstrated, but it was resistant to the regulation of normal Ts. No lymphocytotoxin was demonstrated in IBL serum. The induction of Ts activity by the ConA activation of IBL lymphocytes was markedly decreased. Null lymphocytes of Fr I showed the helper effect to the development of clg+ cells from normal B lymphocytes by the PWM stimulation.抄録全体を表示PDF形式でダウンロード (594K) -
畔柳 武雄, 蔵 和夫, 田中 和也, 荘 茂1980 年 3 巻 4 号 p. 196-204
発行日: 1980/09/30
公開日: 2009/01/22
ジャーナル フリーImmunological studies were carried out on ten patients with the aplastic anemia with hyperplasia of erythroblasts (AAHE). A decrease of E-RFC and Thy+ cells and an increase of Fc (γ) receptor positive (FcR+) cells, Tγ, Tpμ and null lymphocytes were demonstrated in blood lymphocytes of patients with AAHE. Tγ, FcR+ cells and K cells were increased in the bone marrow lymphocytes subpopulation in patients with AAHE. The antibody dependent cell-mediated cytotoxity to patelets, erythroblasts and immature granulocytes was positive in patients with AAHE. Bone marrow lymphocytes from patients with AAHE produced IgG in vitro by the stimulation of platelet membrane antigens, erythroblast membrane antigens and immature granulocyte membrane antigens. A decrease of suppressor T cells (Ts) was present in blood lymphocytes of patients with AAHE. The in vitro development to Ig producing cells of bone marrow lymphocytes by PWM stimulations was increased in AAHE. The sensitivity of bone marrow lymphocytes to normal Ts was decreased in AAHE. These results indicate that AAHE is the autoimmune diseases which might be cause probably by the similar mechanism with that in Hashimoto's thyroidits. AAHE should be termed as the autoimmune pancytopenia.抄録全体を表示PDF形式でダウンロード (501K) -
1.メカニズムの検討余 家利, 谷本 潔昭, 堀内 淑彦1980 年 3 巻 4 号 p. 205-216
発行日: 1980/09/30
公開日: 2009/01/22
ジャーナル フリーヒト末梢血好中球とリンパ球を用て,ニワトリ赤血球をtargetとしてmitogen induced cell-mediated cytotoxicity (MICC)を行った.好中球(PMN)およびリンパ球(PBL)によるMICCは同様のdose response,温度依存性を示し, B-cell mitogenでは誘導されず, T-cell mitogenによってのみ誘導された. PMNはPBLよりも強いcytotoxicityを示した. MICCがおこるためには, effectorとtargetの直接の接触が必要であり,赤血球呑食はMICCに直接関与はしておらず,またeffectorとmitogen, targetの培養上清, PMNの超音波破壊溶解物はMICCに影響がなかった.さらにMICCの阻止試験を行い, MICCのメカニズムの解明を試みた.その結果, membrane active agent, anti-tublin, anti-microfilament, EDTA,局麻剤および可溶性immune complexはMICCを強く抑制した. DNA合成の阻止剤,特異的な単糖類は,中等度の阻止効果を示したが,金塩,不溶性immune complexあるいはmembrane Na+-K+-ATPase inhibitorは, MICCにほとんど効果がなかった.これらの結果は, MICCが十分に発揮されるためには,機能的に正常なレクチンと反応する膜レセプター,正常な細胞骨格系, activeなDNA合成ならびに2価のイオンを必要とすることを結論して示している.抄録全体を表示PDF形式でダウンロード (714K) -
松本 美富士1980 年 3 巻 4 号 p. 217-224
発行日: 1980/09/30
公開日: 2009/01/22
ジャーナル フリーPolymyalgia rheumatica (PMR) was a rare rheumatic disease in Japan, nevertherless common in European and American caucasians. In Japan recently PMR is one of well established rheumatic diseases. We experienced four cases of PMR in our rheumatic clinic for the past five years. Only one of them was male and the youngest case was 41 years of age. Most of them presented with myalgic pains of proximal areas of trunks, continuous fever and emaciation. It took for long time (3 months to 4 years) inorder to diagnose PMR. The previous diagnosis were fever of unknown origin (FUO) or some collagen diseases. One of them was a case associated with temporal arteritis, which was diagnosed from a biopsy finding of temporal artery. Other case was strongly suspected to be associated with temporal arteritis. All of them well responded to corticosteroid administration, and myalgic pain and fever episodes disappered promptly. It was difficult to taper off the corticosteroid in all cases. In serological examination it was showed that one of them had the antibody against DNA.抄録全体を表示PDF形式でダウンロード (1570K) -
押味 和夫, 狩野 庄吾1980 年 3 巻 4 号 p. 225-230
発行日: 1980/09/30
公開日: 2009/01/22
ジャーナル フリーPDF形式でダウンロード (271K)
- |<
- <
- 1
- >
- >|